Curated HPA-Axis Models

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(A mechanistic model of ACTH-stimulated cortisol secretion)
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==A mechanistic model of ACTH-stimulated cortisol secretion==
==A mechanistic model of ACTH-stimulated cortisol secretion==
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Although this model is bit old, it can capture mechanistic behavior of the ACTH stimulated cortisol secretion.  GPCR signaling part is very much outdated and model does not consider the cholesterol uptake through LDL receptors pathway which is crucial for maximal steroid production. In fact Neither endogenous cellular cholesterol synthesis nor mobilization of stored cholesteryl esters is sufficient to support maximal steroid production, since hormone-stimulated steroid production is markedly augmented in the presence of lipoproteins.
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Although this model [1] is bit old, it can capture mechanistic behavior of the ACTH stimulated cortisol secretion.  GPCR signaling part is very much outdated and model does not consider the cholesterol uptake through LDL receptors pathway which is crucial for maximal steroid production. In fact Neither endogenous cellular cholesterol synthesis nor mobilization of stored cholesteryl esters is sufficient to support maximal steroid production, since hormone-stimulated steroid production is markedly augmented in the presence of lipoproteins [2].

Revision as of 16:55, 1 February 2010

A mechanistic model of ACTH-stimulated cortisol secretion

Although this model [1] is bit old, it can capture mechanistic behavior of the ACTH stimulated cortisol secretion. GPCR signaling part is very much outdated and model does not consider the cholesterol uptake through LDL receptors pathway which is crucial for maximal steroid production. In fact Neither endogenous cellular cholesterol synthesis nor mobilization of stored cholesteryl esters is sufficient to support maximal steroid production, since hormone-stimulated steroid production is markedly augmented in the presence of lipoproteins [2].



  1. Dempsher DP, Gann DS, and Phair RD. . pmid:6326602. PubMed HubMed [Dempsher_Gann_Phair_1984]
  2. Kraemer FB, Shen WJ, Patel S, Osuga J, Ishibashi S, and Azhar S. . pmid:16985254. PubMed HubMed [Kraemer_others_2007]
All Medline abstracts: PubMed HubMed
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